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Dietary fat intake, pesticide use, and Parkinson's disease.

Abstract

BACKGROUND

Dietary fat intake may modify Parkinson's disease (PD) risk directly or by altering the response to environmental neurotoxicants including pesticides.

METHODS

We conducted a case-control study of PD nested in the Agricultural Health Study (AHS), a cohort of pesticide applicators and spouses. We evaluated diet and pesticide use before diagnosis in 89 PD cases, confirmed by movement disorder specialists, or a corresponding date in 336 frequency-matched controls. Associations were evaluated using multivariate logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs).

RESULTS

In the AHS, PD was inversely associated with N-3 polyunsaturated fatty acids (PUFAs) (OR 0.4, 95% CI 0.2-0.8 for highest vs. lowest tertile) and the N-3 precursor α-linolenic acid (0.4, 0.2-0.8). In a meta-analysis of nine studies, including the present one, PD was inversely associated with α-linolenic acid (0.81, 0.68-0.96). In the AHS, associations of PD with the pesticides paraquat and rotenone were modified by fat intake. The OR for paraquat was 4.2 (1.5-12) in individuals with PUFA intake below the median but 1.2 (0.4-3.4) in those with higher intake (p-interaction = 0.10). The OR for rotenone was 5.8 (2.3-15) in those with saturated fat intake above the median but 1.5 (0.5-4.2) in those with lower intake (p-interaction = 0.02).

CONCLUSIONS

PUFA intake was consistently associated with lower PD risk, and dietary fats modified the association of PD risk with pesticide exposure. If confirmed, these findings suggest that a diet high in PUFAs and low in saturated fats might reduce risk of PD.

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  • Authors+Show Affiliations

    ,

    Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA. Electronic address: kamel@niehs.nih.gov.

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    The Parkinson's Institute, Sunnyvale, CA, USA.

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    Biostatistics Branch, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC, USA.

    ,

    Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA.

    ,

    Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA.

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    Westat Inc, Durham, NC, USA.

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    The Parkinson's Institute, Sunnyvale, CA, USA.

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    Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada.

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    The Parkinson's Institute, Sunnyvale, CA, USA.

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    Department of Neurology, University of Lübeck, Lübeck, Germany; Department of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany.

    ,

    Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA.

    ,

    The Parkinson's Institute, Sunnyvale, CA, USA.

    ,

    Institute of Cognitive Neurology, Institute of Neuroscience, Favaloro University, Buenos Aires, Argentina.

    ,

    Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, MD, USA.

    ,

    The Parkinson's Institute, Sunnyvale, CA, USA.

    ,

    Veterans Affairs Pacific Islands Health Care System, Honolulu, HI, USA.

    ,

    The Parkinson's Institute, Sunnyvale, CA, USA.

    ,

    Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA.

    The Parkinson's Institute, Sunnyvale, CA, USA.

    Source

    Parkinsonism & related disorders 20:1 2014 Jan pg 82-7

    MeSH

    Adult
    Aged
    Aged, 80 and over
    Case-Control Studies
    Diet
    Dietary Fats
    Fatty Acids, Omega-3
    Female
    Humans
    Male
    Middle Aged
    Parkinson Disease
    Pesticides
    Risk Factors

    Pub Type(s)

    Journal Article
    Meta-Analysis
    Research Support, N.I.H., Extramural
    Research Support, N.I.H., Intramural

    Language

    eng

    PubMed ID

    24120951

    Citation

    TY - JOUR T1 - Dietary fat intake, pesticide use, and Parkinson's disease. AU - Kamel,Freya, AU - Goldman,Samuel M, AU - Umbach,David M, AU - Chen,Honglei, AU - Richardson,Gina, AU - Barber,Marie Richards, AU - Meng,Cheryl, AU - Marras,Connie, AU - Korell,Monica, AU - Kasten,Meike, AU - Hoppin,Jane A, AU - Comyns,Kathleen, AU - Chade,Anabel, AU - Blair,Aaron, AU - Bhudhikanok,Grace S, AU - Webster Ross,G, AU - William Langston,J, AU - Sandler,Dale P, AU - Tanner,Caroline M, Y1 - 2013/10/01/ PY - 2013/6/17/received PY - 2013/9/10/revised PY - 2013/9/23/accepted PY - 2013/10/1/aheadofprint PY - 2013/10/15/entrez PY - 2013/10/15/pubmed PY - 2014/9/13/medline PY - 2015/1/1/pmc-release KW - Dietary fat KW - Parkinson's disease KW - Pesticides KW - Polyunsaturated fatty acids SP - 82 EP - 7 JF - Parkinsonism & related disorders JO - Parkinsonism Relat. Disord. VL - 20 IS - 1 N2 - BACKGROUND: Dietary fat intake may modify Parkinson's disease (PD) risk directly or by altering the response to environmental neurotoxicants including pesticides. METHODS: We conducted a case-control study of PD nested in the Agricultural Health Study (AHS), a cohort of pesticide applicators and spouses. We evaluated diet and pesticide use before diagnosis in 89 PD cases, confirmed by movement disorder specialists, or a corresponding date in 336 frequency-matched controls. Associations were evaluated using multivariate logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: In the AHS, PD was inversely associated with N-3 polyunsaturated fatty acids (PUFAs) (OR 0.4, 95% CI 0.2-0.8 for highest vs. lowest tertile) and the N-3 precursor α-linolenic acid (0.4, 0.2-0.8). In a meta-analysis of nine studies, including the present one, PD was inversely associated with α-linolenic acid (0.81, 0.68-0.96). In the AHS, associations of PD with the pesticides paraquat and rotenone were modified by fat intake. The OR for paraquat was 4.2 (1.5-12) in individuals with PUFA intake below the median but 1.2 (0.4-3.4) in those with higher intake (p-interaction = 0.10). The OR for rotenone was 5.8 (2.3-15) in those with saturated fat intake above the median but 1.5 (0.5-4.2) in those with lower intake (p-interaction = 0.02). CONCLUSIONS: PUFA intake was consistently associated with lower PD risk, and dietary fats modified the association of PD risk with pesticide exposure. If confirmed, these findings suggest that a diet high in PUFAs and low in saturated fats might reduce risk of PD. SN - 1873-5126 UR - https://www.unboundmedicine.com/medline/citation/24120951/full_citation L2 - http://linkinghub.elsevier.com/retrieve/pii/S1353-8020(13)00353-2 ER -